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Emmanuel M Awumey

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Contact Information

Title:
Associate Professor
Email:
eawumey@nccu.edu
Phone:
(919) 530-7644
Fax:
(919) 530-7998
Office:
118 Julius L. Chambers Biomedical/Biotechnology Research Institute (BBRI)

Jobs/Responsibilities

Principle Investigator,
Cardio-Metabolic Diseases Research Program, BBRI

Biography

I hold M.Sc. and Ph.D degrees in Pharmacology from the University of Alberta in Canada. My Ph.D thesis research was on the effects of thyroid hormones and dietary fatty acids on myocardial contractility. My post-doctoral training was in the Department of Medicine at the Medical University of South Carolina in Charleston, where I studied calcium and bone metabolism. After research stints at the MCP Hahnemann University (now Drexel University) and Thomas Jefferson University in Philadelphia, I joined the Cardiovascular Research Program at the Julius L. Chambers Biomedical/Biotechnology Research Institute (JLC-BBRI) at North Carolina Central University as a Research Scientist in May, 2000. I am currently a tenured Associate Professor in the Department of Biological and Biomedical Sciences and an adjunct faculty at the Hypertension & Vascular Research Center and the Department of Physiology & Pharmacology at the Wake Forest University School of Medicine.
The focus of my research at the JLC-BBRI is to investigate the mechanism of perivascular nerve Ca2+-sensing receptor (CaSR) signaling and vasodilation and its modulation in hypertension. Our laboratory pioneered the research on this novel receptor and proposed that its activation leads to the release of vasodilator substances in resistance arteries. Over the past seventeen years, we have carried out uninterrupted research on this subject. Since joining the JLC-BBRI as a Research Scientist, I have cloned the receptor from dorsal root ganglia, expressed it in HEK293 cells and characterized its activation and signaling that leads to release of stored Ca2+. These studies yielded several publications and the data were used to obtain an SC1 grant from NHLBI for 5 years. I have successfully directed studies in an R01 grant (awarded to my late mentor), which explored the linkage between Ca2+ homeostasis and vascular tone. These ex vivo studies employed mesenteric arteries from rats to elucidate the pathways of CaSR signaling and release of vasodilators. We have expanded these studies to Dahl salt-sensitive (SS) and salt-resistant (SR) rats as well as nitric oxide (NO) synthase (NOS) knockout mice, two animal models of hypertension. In SS rats, a high salt diet (8%NaCl) up-regulated CaSR expression in kidney and the mesenteric arteries. The data suggest up-regulation in the mesentery correlates with CaSR-mediated relaxation. eNOS knockout also up-regulates but nNOS knockout down-regulates the CaSR in mesenteric arteries, and eNOS-derived NO enhanced Ca2+-induced vasorelaxation.
In collaboration with the Gene Editing Rat Research Center at the Medical College of Wisconsin, we have now developed an SS rat model with a mutated CaSR gene to study the physiological role of the receptor in salt-sensitive hypertension, a disease prevalent in the African American community. I have recently been awarded a second SC1 grant for 4 years for this study.

Research Interests

Characterization of the signaling mechanisms of the perivascular nerve calcium-sensing receptor (CaSR) with a long term goal of elucidating its role in vasodilation, hence blood pressure regulation. We focus on the molecular mechanisms linking Ca2+ homeostasis and vascular function in salt-sensitive hypertension. We are carrying out studies with isolated resistance arteries from nitric oxide synthase (NOS) knockout mice, Dahl salt-sensitive (SS) and salt-resistant (SR)rats, and SS rats with the mutated CaSR to determine the effects of these manipulations on CaSR signaling pathways that result in Ca2+e-induced blood vessel relaxation. We anticipate that these studies will lead to understanding of the molecular mechanisms linking Ca2+ homeostasis and vascular function and may provide the basis for the development of novel pharmacologic means of regulating blood pressure in salt-sensitive hypertension that is prevalent in the African-American community.

Education

PhD University of Alberta 1993
MS University of Alberta 1989

Vita/Resume

Download PDF

Selected Publications

1. Sesay, J. S., & Gyapong, R. N., & Najafi, L. T., & Kabler, S. L. (2015). G?i/o-dependent Ca2+ mobilization and G?q-dependent PKC? regulation of Ca2+-sensing . Neurochem. Int., 90, 142-151.
2. Awumey, E. M., & Bridges, L. E., & Williams, C. L., & Diz, D. I. (2013). Nitric oxide synthase knockout modulates Ca2+-sensing receptor expression and signaling in mouse mesenteric arteries.. J Pharmacol Exp Ther, 38-47.
3. Awumey, E. M., & Hill, S. K., & Bukoski, R. D. (2008). Cytochrome P-450 metabolites of. Am J Physiol Heart Circ Physiol. , 294, 2363-2370.
4. Heyeraas, K. J., & Huang, S. R., & Bukoski, R. D., & Awumey, E. M. (2008). Identification of a Ca2+-sensing receptor in rat trigeminal ganglia, sensory neurons, and dental pulp.. Calcif Tissue Int., 82, 57-65.
5. Awumey, E. M., & Howlett, A. C., & Putney, J. W., & Diz, D. I. (2007). Ca2+ mobilization through dorsal root ganglion Ca2+-sensing receptor stably expressed in HEK293 cells. Am J Physiol Cell Physiol, 292, 1895-1905.
6. Wang, Y. , & Awumey, E. M., & Chaterjee, P. K., & Bukoski, R. D. (2003). Molecular cloning and characterization of a rat sensory nerve Ca2+-sensing receptor. Am J Physiol Cell Physiol, 285, 64-75.
 
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